Linked Life Data

21324712

Source:http://linkedlifedata.com/resource/pubmed/id/21324712

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-3-30
pubmed:abstractText
Histamine is a biological amine that plays an important role in allergic responses. However, the involvement of histamine signaling in late allergic responses in the skin is poorly understood. Therefore, we attempted to investigate the involvement of histamine signaling in late allergic responses, especially in keratinocytes (KCs). HaCaT KCs and normal human KCs (NHKs) predominantly expressed histamine H1 receptor (H1R) and H2 receptor (H2R). Histamine suppressed tumor necrosis factor ? (TNF-?)- and interferon-? (IFN-?)-induced production of CC chemokine ligand 17(CCL17), a type 2 T-helper (Th2) chemokine, by HaCaT KCs. It suppressed the phosphorylation of p38 mitogen-activated protein (MAP) kinase, but not that of extracellular signal-regulated kinases (ERKs), and TNF-?- and IFN-?-induced nuclear factor ?B (NF?B) activity. In contrast, histamine enhanced the production of CXC chemokine ligand 10 (CXCL10), a Th1 chemokine, by TNF-?- and IFN-?-stimulated HaCaT KCs and NHKs. TNF-?- and IFN-?-induced CXCL10 production was upregulated by suppression of p38 MAP kinase or NF-?B activity, which could explain histamine involvement. We concluded that histamine suppresses CCL17 production by KCs by suppressing p38 MAP kinase and NF-?B activity through H1R and may act as a negative-feedback signal for existing Th2-dominant inflammation by suppressing CCL17 and enhancing CXCL10 production.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1096-0023
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
191-9
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Histamine differentially regulates the production of Th1 and Th2 chemokines by keratinocytes through histamine H1 receptor.
pubmed:affiliation
Department of Dermatology, University of Tokyo, Tokyo, Japan.
pubmed:publicationType
Journal Article